Secher NH, Seifert T, Van Lieshout JJ. Cerebral blood flow and metabolism during exercise, implications for fatigue. J Appl Physiol 104: 306 -314, 2008. First published October 25, 2007 doi:10.1152/japplphysiol.00853.2007.-During exercise: the Kety-Schmidt-determined cerebral blood flow (CBF) does not change because the jugular vein is collapsed in the upright position. In contrast, when CBF is evaluated by 133 Xe clearance, by flow in the internal carotid artery, or by flow velocity in basal cerebral arteries, a ϳ25% increase is detected with a parallel increase in metabolism. During activation, an increase in cerebral O 2 supply is required because there is no capillary recruitment within the brain and increased metabolism becomes dependent on an enhanced gradient for oxygen diffusion. During maximal whole body exercise, however, cerebral oxygenation decreases because of eventual arterial desaturation and marked hyperventilation-related hypocapnia of consequence for CBF. Reduced cerebral oxygenation affects recruitment of motor units, and supplemental O 2 enhances cerebral oxygenation and work capacity without effects on muscle oxygenation. Also, the work of breathing and the increasing temperature of the brain during exercise are of importance for the development of so-called central fatigue. During prolonged exercise, the perceived exertion is related to accumulation of ammonia in the brain, and data support the theory that glycogen depletion in astrocytes limits the ability of the brain to accelerate its metabolism during activation. The release of interleukin-6 from the brain when exercise is prolonged may represent a signaling pathway in matching the metabolic response of the brain. Preliminary data suggest a coupling between the circulatory and metabolic perturbations in the brain during strenuous exercise and the ability of the brain to access slow-twitch muscle fiber populations. ammonium; central fatigue; cerebral blood flow; cerebral metabolic ratio; glucose; glycogen; lactate; oxygen; temperature DURING EXERCISE, THERE IS hyperbolic relationship between work intensity and endurance, and A. V. Hill used the relationship to demonstrate that energy turnover can be taken to represent a continuous provision of energy supplemented by an energy store (56). Yet, it is the brain that makes the decision when to slow down or to stop exercise, and from that perspective fatigue is of central origin. Obviously, cerebral metabolism becomes affected if exercise has a duration that lowers blood glucose (74), and, equally, the low O 2 tension faced during mountaineering (47) affects brain function. Perturbation of cerebral metabolism is, however, not restricted to situations where the arterial glucose and O 2 levels are reduced. Recent investigations (3,65,70,90) indicate that also at sea level maximal exercise may be associated with so-called central fatigue as indicated by lower voluntary activation than the force elicited during evoked contractions.The purpose of this review is to address cerebral metabolism in ...

The circulating level of brain-derived neurotrophic factor (BDNF) is reduced in patients with major depression and type-2 diabetes. Because acute exercise increases BDNF production in the hippocampus and cerebral cortex, we hypothesized that endurance training would enhance the release of BDNF from the human brain as detected from arterial and internal jugular venous blood samples. In a randomized controlled study, 12 healthy sedentary males carried out 3 mo of endurance training (n = 7) or served as controls (n = 5). Before and after the intervention, blood samples were obtained at rest and during exercise. At baseline, the training group (58 + or - 106 ng x 100 g(-1) x min(-1), means + or - SD) and the control group (12 + or - 17 ng x 100 g(-1) x min(-1)) had a similar release of BDNF from the brain at rest. Three months of endurance training enhanced the resting release of BDNF to 206 + or - 108 ng x 100 g(-1) x min(-1) (P < 0.05), with no significant change in the control subjects, but there was no training-induced increase in the release of BDNF during exercise. Additionally, eight mice completed a 5-wk treadmill running training protocol that increased the BDNF mRNA expression in the hippocampus (4.5 + or - 1.6 vs. 1.4 + or - 1.1 mRNA/ssDNA; P < 0.05), but not in the cerebral cortex (4.0 + or - 1.4 vs. 4.6 + or - 1.4 mRNA/ssDNA) compared with untrained mice. The increased BDNF expression in the hippocampus and the enhanced release of BDNF from the human brain following training suggest that endurance training promotes brain health.

No abstract

Isolated activation of metabolically sensitive skeletal muscle afferents (muscle metaboreflex) using post-exercise ischaemia (PEI) following handgrip partially maintains exercise-induced increases in arterial blood pressure (BP) and muscle sympathetic nerve activity (SNA), while heart rate (HR) declines towards resting values. Although masking of metaboreflex-mediated increases in cardiac SNA by parasympathetic reactivation during PEI has been suggested, this has not been directly tested in humans. In nine male subjects (23 ± 5 years) the muscle metaboreflex was activated by PEI following moderate (PEI-M) and high (PEI-H) intensity isometric handgrip performed at 25% and 40% maximum voluntary contraction, under control (no drug), parasympathetic blockade (glycopyrrolate) and β-adrenergic blockade (metoprolol or propranalol) conditions, while beat-to-beat HR and BP were continuously measured. During control PEI-M, HR was slightly elevated from rest (+3 ± 2 beats min −1 ); however, this HR elevation was abolished with β-adrenergic blockade (P < 0.05 vs. control) but augmented with parasympathetic blockade (+8 ± 2 beats min −1 , P < 0.05 vs. control and β-adrenergic blockade). The HR elevation during control PEI-H (+9 ± 3 beats min −1 ) was greater than with PEI-M (P < 0.05), and was also attenuated with β-adrenergic blockade (+4 ± 2 beats min −1 , P < 0.05 vs. control), but was unchanged with parasympathetic blockade (+9 ± 2 beats min −1 , P > 0.05 vs. control). BP was similarly increased from rest during PEI-M and further elevated during PEI-H (P < 0.05) in all conditions. Collectively, these findings suggest that the muscle metaboreflex increases cardiac SNA during PEI in humans; however, it requires a robust muscle metaboreflex activation to offset the influence of cardiac parasympathetic reactivation on heart rate.